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marylin monroe
Showing posts with label ergogenics. Show all posts
Showing posts with label ergogenics. Show all posts

Bicarbonate For Strength Athletes: 25g of Baking Soda Up Your Squat (+27%) & Bench Press (+6%) Within 60 Min

NaHCO3 probably won't make the burn go away, but it will help you push though it.... and no(!), you don't have to be afraid to retain water - sodium bicarbonate is actually going to lower aldosterone and is thus - if anything - going to have a diuretic effect (Musabayane. 1991). Calcium loss etc. is nothing you have to be afraid of either (Luft. 1990).
After yesterday's astonishingly popular excursion into dating sciences, we are back to "normal" or as others would call it "extraordinary", here at the SuppVersity today ;-) And to make really sure you know that you're right here we're going to get back into the ergogenic groove with one of my personal favorites: Sodium bicarbonate, NaHCO3 or as your granny calls it, baking soda!

In the unfortunate case you have no idea, what I am taking about, I'd suggest you briefly go through the previous SuppVersity articles and Facebook posts (e.g. +13% increase the sprinting capacity; sorry for the → typo) about the ergogenic effects of baking soda . Once you've done that it should not really come as a surprise that scientists from the real Human Performance Laboratory  at the Coventry University in the UK found that NaHCO3 will not just for cyclists, runners and rowers, but also for "bench pressers" and "squatters" ;-)

One thing after the other, though!

If you know your SuppVersity articles by heart, you are probably thinking about the Kerr study from September 2012, now - right? For the average gymrat, this was probably the most exciting paper on the ergogenic effects of sodium bicarbonate supplementation I've written about (see "22g Baking Soda 60min Before a Old-School 4 x 12RM Leg Workout Allow for a 22 Rep Volume Increase on Hypertrophy Oriented Squat + Leg Press + Leg Extension Quads Routine" | read more).
A note for those with gastrointestinal problems or an insurmountable gag reflex: I know that downing 25g sodium bicarbonate at once can be disgusting and sends people with weaker stomachs right to the toilette. Fortunately, a 2012 study by Dreher et al. suggests that "serial loading" with several smaller servings of baking soda works at least as well | learn more
And while the Kerr study was among the first to demonstrate significant beneficial effects of sodium bicarbonate in a strength training scenario, it is - if you come to think of it, actually not that surprising to see that the H+ (=hydrogen ions → acidity) buffering effect works just as well during a high volume leg workout, as it does, during high intensity cycling and sprinting [just a note on the H+ buffer: contrary to beta alanine, bicarbonate buffers the acidity in the blood, not within the muscle cell and will thus have greater effects on the periphery than carnosine the histidine + beta alanine dipeptide you are actually looking for, whenever you take your beta alanine supplement.

Now while it may not have been surprising that high volume + baking soda does make a perfect match, it is, as you will hopefully agree, not exactly straight forward that we would see similar benefits on the low volume performance test, the 8  men (mean age, height and body mass → 20  ±0.9 years, 1.8  ± 0.1m and 78.4  ± 15.6kg, respectively)  who had been recruited for the study at hand had to perform.

Three sets of squats and bench presses? Isn't that too little volume for NaCO3 to work?

All the participants who had at least one year of strength training experience competed  in  team  games  (rugby  union,  soccer, basketball) at the national level and were concomitantly training more than 10 hours per week as part of their regular preseason preparations (those included 3h of resistance training). During the testing conditions to which the subjects had been randomly assigned, all of the performed
Learn about the best chest exercises in the SuppVersity EMG Series.
  • three sets of bench presses to failure at 80% 1RM, and 
  • three sets of back squats "to failure" at 80% 1RM
With three minutes of rest between the sets and five minutes of rest between exercises, this is, as I already mentioned, not exactly the workout you would usually expect to benefit (most) from bicarbonate supplementation. Still, the data in Figure 1 tells another story:
  • 0.3g/kg NaHCO3 in 5 ml/kg of artificially sweetened water (NaHCO3), instead of
  • 0.045g/kg NaCL in an artificially sweetened water drink matched for taste
60 minutes before the two blinded performance tests did the trick - it did increase the mean total reps for squats (+6.7 reps; +27%) and bench preses (+1.5 reps; +6% -- note: I used the values from the table in the full text. They differ from those in the abstract according to which the performance increase would be 7%)
Figure 1: Back squat and bench press performance in three subsequent sets (Duncan. 2013)
As it was to be expected due to the low volume and long rest between sets, there was no significant change in blood lactate across time or between conditions. There were however treatment × time interactions for blood pH (p = 0.014) and blood HCO3 concentration (p = 0.001), with the increasing pH and bicarbonate (HCO3) levels in the blood of the NaHCO group being the obvious cause of the highly significant performance benefits.
Does beta alanine hamper instead of improve your sprinting performance? Learn more in a previous SV Article.
Baking soda for strength athletes: After the previously cited study by Kerr et al. this is study #2 to prove that the usefulness of baking soda, sodium bicarbonate or NaHCO3 (call it whatever you want) is by no mean, as it was long thought to be, restricted to endurance sports with intermittent sprints. With the study at hand there is enough evidence to believe that it's acute effects are going to be present whenever you're pushing yourself to your own limits and in view of the fact that pushing to the limits, in order to raise the bar is what's driving progress.

I would therefore be curious to see a long(er) term study (8-12 weeks) taking a look at the cumulative benefits of sodium bicarbonate supplementation on strength and mass gains in trained and untrained individuals. Unfortunately, I suppose that no one with the money to finance that study will share my interest. In the end, a study like this would after all entail the risk of exposing how pathetic the 2.85% performance increase we see in the average beta alanine study actually are (Hobson. 2012).
    Reference: 
    • Duncan MJ, Weldon A, Price MJ. The effect of sodium bicarbonate ingestion on back squat and bench press exercise to failure. J Strength Cond Res. 2013 Oct 11. [Epub ahead of print]
    • Hobson RM, Saunders B, Ball G, Harris RC, Sale C. Effects of β-alanine supplementation on exercise performance: a meta-analysis. Amino Acids. 2012 Jul;43(1):25-37. 
    • Luft FC, Zemel MB, Sowers JA, Fineberg NS, Weinberger MH. Sodium bicarbonate and sodium chloride: effects on blood pressure and electrolyte homeostasis in normal and hypertensive man. J Hypertens. 1990 Jul;8(7):663-70.
    • Musabayane CT, Balment RJ. Renal effects of aldosterone in the sodium bicarbonate infused rat. Ren Fail. 1991;13(2-3):71-6.

    New Role for Glutamine in Protein Synthesis? Study Suggests Direct Effects on Mammalian Target of Rapamycin (mTOR) - EAAs Alone Won't Produce Optimal Results

    Image 1 (Pumping Iron): The guy in the middle, obviously no one else than the Austrian Oak, took glutamine, the rest of the guys forgot about it in all the craze about leucine... no, just kiddin' ;-) Still, someone who trains like Arnold, is probably most likely to benefit from additional l-glutamine
    After all those bad news about allegedly effective supplements, I thought it may be about time to present some good news about an allegedly ineffective supplement: Glutamine! Published ahead of print in the online version of the scientific journal Amino Acids, the results from a 2012 study by Martina Chiu and her colleagues from the Unit of General and Clinical Pathology at the Department of Experimental Medicine of the University of Parma in Italy (Chia. 2012), could well explain a recent comment by Macijec who recounts that he saw great improvements in lean-mass retention on a diet from a combined BCAA + glutamine supplement over taking just plain BCAAs. And while I will get to what I believe is a much more likely explanation for this observation in the conclusion of this blogpost, let's initially take a look at what Chiu et al. bring to the table.

    Don't take away my glutamine, man!

    Previous studies by Evans et al. had already suggested that glutamine, despite its non-essential nature (meaning that your body can produce it from other amino acids by transamination), plays more than just a facilitative role in the phosphorylation of  the mammalian target of rapamycin (mTOR) and skeletal muscle protein synthesis (Evans. 2007 & 2008). To investigate this hypothesis further Chia et al. incubated HepG2 and HeLa cells (the use of these durable and cheap cells instead of myocytes as they were used by Evans, for example, is certainly a downside of the study) and found that
    • the presence / abundance of glutamine influences mTORC1 activity 
    • this effect is not mediated by glutamine induced increases in cellular leucine content
    • the quantitative contribution of leucine and glutamine to the mTORC1 activation is cell-line specific
    • even in the absence of glutamine, mTORC1 activity was not completely suppressed 
    • in all cells both glutamine and leucine appear necessary for the maximal stimulation of mTORC1 
    The cell-line specificity, is unequestionably problematic, still the general finding that glutamine depletion does not lead to a subsequent depletion or lack of uptake of EAAs, which would then in turn reduce the mTOR-induced phosphorylation of the protein uptake regulating enzyme p70S6K (Ribosomal protein S6 kinase beta-1) is probably valid for muscle cells as well. This suggests that" the signals and transduction pathways involved may be also distinct and their sensitivities different." (Chiu. 2012)

    So what does that mean? To take or not to take glutamine - this is the question!

    If we discard that the exact mechanism behind these observation still remains to be elucidated and invoke that there was a biphasic reaction to glutamine depletion with a minimum from 3h-6h and a subsequent partial rescue pf p70SK activity later, these results would support the value of the ingestion of supplemental glutamine particularly right after intense workouts or in periods of caloric restriction, where the intramuscular glutamine and EAA pools (muscle, liver, intestines) are drawn upon also as a substrate for hepatic glycogenesis (=production of sugar in the liver) and exogenous glutamine may spare "pro-anabolic" BCAAs/EAAs (Holecek. 2002).

    Figure 1: Glutamine synthesis
    (Self. 2004)
    The study at hand, as well as the findings of Candow et al. who report a slight, but eventually negligibly greater increases in lean mass (+0.3%) and strength with 0.9g/kg glutamine supplementation over a 0.9g/kg bw. maltodextrin control in the absence of dietary restrictions do yet suggest that the effects of glutamine cannot be explained solely based on its energy content. And would warrant further investigations into what would be the threshold and optimal EAA and glutamine levels to propel skeletal muscle protein synthesis in vivo and whether or not, a energetically non-restricted high protein diet alone will not eventually provide enough glutamine and respective substrates for it's "on demand" production (cf. figure 1)

    Are you training hard to be "glutamine deficient"?

    That in fact the intensity of your exercise regimen may be the fundamental determinant of whether you do or don't need supplemental l-glutamine would be supported by the well-established efficiacy of parentally administered glutamine to critically ill patients. As so often inflammation appears to be, once again, the fundamentally important determinant, as it has been shown to increase in the net release of glutamine from peripheral tissues, such as your muscles, to central tissues and complex systems like the immune system  the liver (as mentioned before), the spleen (!) and wounds (Soeters. 2012). Against that background the longstanding practice of ingesting extra amounts of glutamine may well make sense, if the latter would actually make it to the periphery and would not be absorbed by exactly those previously enumerated "central tissues" that do not just need it the most, but that have a relatively comprehensive amount of scientific data to back the usefulness of glutamine as well as glutamine-(di-)peptides such as l-alanylglutamine (brand name Sustamine).
    Are those dipeptides so much better? You will probably have heard about the "unbelievable", "unique" and "far superior effects" of glutamine dipeptides compared to the regular, dirt cheap free-form l-glutamine. And despite the fact that I am not aware of studies that would compare one to the other in a relevant, exercise related context, these statements do actually have a rationale basis. After all, the transport of intact peptides by the PEPT transporters in the gastrointestinal tract peptides has the major advantage that the cells of the gut do not avail themselves of as much glutamine as they want before it even reaches systemic circulation (Adibi. 1997). Whatever it's exact effects on protein synthesis may be - on a gram per gram base the dipeptides will therefore be more effective than regular l-glutamine. What you should keep in mind though is that you get both glutamine and alanine from sustamine at a ratio of ~3:2. The 40% of alanine are yet by no means useless. Rather, they could, in and out of themselves, exert (if nothing else) EAA and even glutamine sparing effects, since alanine is, next to lactate and pyruvate, the major gluconeogenic precursor during exercise (Brooks. 1987).
    Image 2: I what's on this tummy is all you put in your tummy, l-glutamine alone will probably not prevent the highly undesirable transition from slightly chubby to skinny fat. With a dialed in, but calorically and/or carb restricted diet, l-glutamine supplementation could yet spare help you spare tissue protein, get rid of ammonia and maintain a decent amount of muscle.
    The two exercise related studies on the latter by Hoffmann et al., which showed beneficial effects of l-alanylglutamine (AG) supplementation on hydration stress during endurance exercise and overall performance during a basketball match do yet suffer from a non-negligible methodological shortcoming: In both trials the AG solution was compared to plain water instead of an isocaloric carbohydrate solution. Against the background hat glutamine and alanine the individual amino acids the peptide is made of are the main substrates for amino acid driven hepatic gluconeogenesis it is at least very questionable whether the observed effects could not have been achieved by the same amount of plain table sugar, since both the  time to exhaustion during a mild hydration stress (Hoffmann. 2010) and the skill performance and visual reaction time (Hoffnmann. 2012) are unquestionably unrelated to the mTOR effects Chiu et al. observed in their study. 

    It would thus warrant a longitudinal study in resistance trained individuals consuming a high protein diet on a high volume strength training regimen (>3 sessions per day, which is the maximum I have come across in hitherto published trials), to see whether your gains would benefit from additional glutamine... if you are dieting, on the other hand, you could argue that you better play safe than be sorry and add another tablespoon of glutamine to your BCAAs ;-)

    References:
    1. Adibi SA. The oligopeptide transporter (Pept-1) in human intestine: biology and function. Gastroenterology. 1997 Jul;113(1):332-40. 
    2. Brooks GA. Amino acid and protein metabolism during exercise and recovery. Med Sci Sports Exerc. 1987 Oct;19(5 Suppl):S150-6.
    3. Candow DG, Chilibeck PD, Burke DG, Davison KS, Smith-Palmer T. Effect of glutamine supplementation combined with resistance training in young adults. Eur  J Appl Physiol. 2001 Dec;86(2):142-9.
    4. Chiu M, Tardito S, Barilli A, Bianchi MG, Dall'asta V, Bussolati O. Glutamine stimulates mTORC1 independent of the cell content of essential amino acids. Amino Acids. 2012 May 8. [Epub ahead of print]
    5. Evans K, Nasim Z, Brown J, Clapp E, Amin A, Yang B, Herbert TP, Bevington A. Inhibition of SNAT2 by metabolic acidosis enhances proteolysis in skeletal muscle. J Am Soc Nephrol. 2008 Nov;19(11):2119-29. Epub 2008 Jul 23. 
    6. Evans K, Nasim Z, Brown J, Butler H, Kauser S, Varoqui H, Erickson JD, Herbert TP, Bevington A. Acidosis-sensing glutamine pump SNAT2 determines amino acid levels and mammalian target of rapamycin signalling to protein synthesis in L6 muscle cells. J Am Soc Nephrol. 2007 May;18(5):1426-36. Epub 2007 Apr 11. 
    7. Holecek M. Relation between glutamine, branched-chain amino acids, and protein metabolism. Nutrition. 2002 Feb;18(2):130-3. 
    8. Self JT, Spencer TE, Johnson GA, Hu J, Bazer FW, Wu G. Glutamine synthesis in  the developing porcine placenta. Biol Reprod. 2004 May;70(5):1444-51. Epub 2004 Jan 21. 
    9. Soeters PB, Grecu I. Have we enough glutamine and how does it work? A clinician's view. Ann Nutr Metab. 2012;60(1):17-26. 

    Caffeine - 3mg, 6mg or 9mg/kg? What's the Optimal Dosage for Lifting & HIT Cycling and What About the Side Effects?

    Wouldn't a single 200mg caffeine be enough to elicit the desired ergogenic effects without side effect like increased urination, headaches and muscle aches on the day after?
    Caffeine is not only the world's #1 it is probably also the most (ab-)used ergogenic on the planet and whatever you may think about the longterm consequences of its use, there is not debating that it is part of those few "supplements" that actually work "no hype, no *bs*" ;-)

    That being said, you may have noticed with yourself that its effect are dose dependent, but not linearly and that some things, such as an increase in mental focus at work require much lower doses of C8H10N4O2 aka 1,3,7-trimethyl-1H-purine-2,6(3H,7H)-dione or 3,7-dihydro-1,3,7-trimethyl-1H-purine-2,6-dione than the elucidation of a major buzz before an intense strength workout.

    So what's the perfect dose, then?

    Without wanting to hurt your feelings, you may imagine that you are not the only one who has come to this realization. In fact, the very same thought must have occurred to Jesús G. Pallarés and his colleagues from the University of Castilla-La Mancha and the Spanish Antidoping Agency, as well. With a whole host of technological equipment and the money to conduct a study with thirteen highly resistance train men (age 21.9 ± 2.9; 76.5 ± 8.5 kg, height 172.7 ± 5.4 cm, body fat 12.4 ± 2.7), the Spanish scientists are yet in a much better position to elucidate where exactly these sweet spots would be.
    Figure 1: Illustration of the procedure on the testing days (Pallarés. 2013)
    To this ends, Pallarés et al. had their volunteers undergo a battery of muscle strength and power tests, namely a  free-weight fullsquat (SQ) and bench press (BP) exercises against  4 incremental loads (25%, 50%, 75% and 90% 1RM), as well as a test in which their cycling peak power output (PPO) was measured using a 4s inertial load test in a randomized in a double-blind, cross over design.

    On the four separate testing days, the subjects ingested either a placebo supplement (PLAC) or, caffeine at dosages of ...
    • 3mg/kg body weight (CAFF3mg), 
    • 6mg/kg body weight (CAFF6mg) and
    • 9mg/kg body weight (CAFF9mg)
    The day before and during the seven days that the experiment lasted, the subjects lived at the sports performance center where they slept and ate all meals. They all consumed a diet of 2800-3000 kcal·day/day that had a macronutrient make-up where 55% energy intake came from carbohydrates, 25% from fat and 20% from protein. The energy intake was evenly distributed across three meals each day (breakfast at 7:00 a.m., lunch at 13:30 p.m. and dinner at 20:00 p.m.). Subjects refrained from physical activity other than that required by the experimental trials, and withdrew from alcohol, tobacco and any kind of caffeine intake 10 days before testing and while the experiment lasted.

    On the actual testing day some baseline measurements, such as height, body fat %, as well as blood and urine samples were taken (PRE). Afterwards the subjects consumed a standardized "breakfast" consisting of a 330 mL of fruit milkshake (168 kcal) and a pastry (456 kcal; total energy for both 624 kcal; 68 g of carbohydrates) along with the their individualized randomized caffeine dose (3, 6 or 9 mg/kg) or placebo in capsule form. After this "delicious" *lol* breakfast, the participants performed
    "[...] a standardized warm-up that consisted of 10 min of jogging at 10 km/h and 10 min of static stretches and joint mobilization exercises, the subjects entered the laboratory to start the neuromuscular test battery assessments under a paced schedule (see figure 1).  These tests consisted of the measurement of bar displacement velocity and muscle power output against 4 incremental loads (25%, 50%, 75% and 90% of 1RM) for upper and lower body musculature (BP and SQ).  Those step measures allowed a continuous representation of the load-velocity and load-power curves to study the interaction between load and caffeine dose on neuromuscular performance.  Cycling peak power output (PPO) was assessed next using a nonfatiguing inertial load test of 4 s duration.  Subjects remained blinded to the results during the whole experiment. Instructions prior to lifting were standardized and always delivered by the same experimenter.
    The whole procedure took about 60min and upon completion of the test battery a second  urine  and  blood  sample  was  collected  (POST). Moreover, all participants were required to fill out an obligatory questionnaire (QUEST+0h) that was aimed to address whether side-effects of caffeine were present during the trial.

    Caffeine a side effect free ergogenic? Not exactly, no...

    As some of you may know from their own lingering experience things that work, usually don't do that without side effects and the study at hand confirmed that this is no different for caffeine. Somewhat surprisingly, though the side effects the subjects who had refrained from caffeine intake for at least 10 days before the the first test, reported "very similar side effects" for the medium and high dose caffeine trials:
    • a limited increase in the sensations of tachycardia and heart palpitations,
    • self-reported urine output and gastrointestinal problems (8% of the subjects)
    At the same time, the subject’s perception of performance and vigor increased 5 to 7 times above PLAC during the CAFF 3mg and CAFF6mg trials (38% and 54% of the subjects, respectively), which would appear to be well worth the minor problems.

    Figure 2: Overview over the number of participants reporting side effects / perceived ergogenic effects (Pallarés. 2013)
    In the course of the 9mg trial (remember: this was a bolus of 693mg caffeine for the average study participant) the men did yet report a "drastic increase" of side-effects (Table 1), of which the researchers consider the reported increase in the estimates of urine output and gastrointestinal problems (62% and 31%, respectively) to be most important. So important, in fact that it is questionable whether that was worth the increased perception of performance and vigor or activeness of 62% and 54%.

    On the subsequent day, participants in the CAFF6mg trials were complaining of increased muscle soreness, headaches and an increase in the estimates of urine output in comparison to the PLAC and CAFF3mgtreatments. Sleep problems and persistently increased vigor occurred only in the  CAFF6mg an CAFF9mg trials with a much higher incidence (23-54% vs. 8% in the high vs. medium dose trial).

    What Pallarés et al. find particularly noteworthy is that "23% of participants reported tachycardia and anxiety or nervousness, 38% with gastrointestinal problems and 54% with insomnia or sleep disturbances" (Pallarés. 2013). This is also the main reason that the researchers recommend "administering the minimal ergogenic dose". But what exactly is this dosage?

    What delivers the most bang with the least side effects?

    In order to answer this question we will have to take a closer look at the performance measures and compare the increases in mean propulsive velocity and muscle power, as well as the cycling PPO and the likelihood and severity of side effects for all four dosing regimen (see figure 3)
    Figure 3: Propulsive velocity during bench presses (left) and propulsive power during bench presses and squats (right) in the placebo, 3mg, 6mg and 9mg trials (Pallarés. 2013)
    As the data in figure 3 goes to show you, caffeine produced ergogenic effects at all dosages. With the heaviest weights, however, the propulsive velocity during bench presses and the squat power required the side-effect laden 9mg dose of caffeine to reach statistical significance. The same goes for the cycling peak power output (not shown).

    Suggested read: "Coffee - The Good, The Bad & The Interesting: 2-4 Cups of Coffee for Adiponectin. Roasted Filtered Coffee & High LDL!? The Optimal Caffeine / Taurine Ratios & the Buzz ". Could taking taurine ameliorate w/out compromising the benefits of caffeine (read more)?
    Bottom line: The study at hand is actually a good example of the myriad of cases, where statistical significance and the real world collide. Let's take another look at the results in figure 3 and the side effects in figure 2. Assuming that you have not whacked your adrenal gland to an extend that you don't respond to caffeine any longer (in that case you better stop taking it all along, anyway), there clearly is no reason to even remotely consider taking caffeine in dosages of more than 6mg/kg body weight before a workout (personally I have found that anything beyond 200-300mg will - in the long run do more harm than good for me, but I guess this really depends on the individual).

    Aside from the subjective side-effects the latter has also been shown to have profoundly detrimental effects on the cortisol to testosterone ratio after a workout (cf. "Revisited: Caffeine's Dose-Dependent Effects on the Testosterone to Cortisol Response to Exercise"; read more)...

    ... and yes, I know that the relevance of this ratio in terms of the "productivity" of your workouts is highly questionable, the latter has been proven for a normal, non-stimulant based increase in cortisol / testosterone, not for the exorbitant increase in cortisol Beavan et al. observed in their 2008 study. If you add the detrimental down-stream effects of messed up sleep, and the obvious dehydration that follows the increased urination observed in the study at hand - overdosing may thus well turn the "proven ergogenic" caffeine into a highly ergolytic agent.

    References:
    • Beaven CM, Hopkins WG, Hansen KT, Wood MR, Cronin JB, Lowe TE. Dose effect of caffeine on testosterone and cortisol responses to resistance exercise. Int J Sport Nutr Exerc Metab. 2008 Apr;18(2):131-41. 
    •  Pallarés JG, Fernández-Elías VE, Ortega JF, Muñoz G, Muñoz-Guerra J, Mora-Rodríguez R. Neuromuscular Responses to Incremental Caffeine Doses: Performance and Side Effects. Med Sci Sports Exerc. 2013 May 10.